Neural mechanisms and management of obesity-related hypertension.
The sympathetic nervous system is activated in human obesity and in the analogous experimental obesity produced by overfeeding. The causes remain uncertain and may be multiple. The consequences include hypertension, probably attributable to activation of the sympathetic outflow to the kidneys, and, more disputed, insulin resistance. The pattern of sympathetic activation in normal-weight and obesity-related hypertension differs in terms of the firing characteristics of individual sympathetic fibers (increased rate of nerve firing in normal-weight hypertensives, increased number of active fibers firing at a normal rate in obesity-hypertension) and the sympathetic outflows involved. The underlying mechanisms and the adverse consequences of the two modes of sympathetic activation may differ. Should antihypertensive drug therapy in obesity-hypertension specifically target the existing neural pathophysiology? Such an approach can be advocated on theoretical grounds. Perhaps more important is the requirement that chosen antihypertensives do not cause weight gain or insulin resistance.
Esler
Murray D
MD
Baker IDI Heart and Diabetes Institute, PO Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia. Murray.Esler@bakeridi.edu.au
Eikelis
Nina
N
Lambert
Elisabeth
E
Straznicky
Nora
N
D058667:Adrenergic beta-3 Receptor Agonists; D006801:Humans; D006946:Hyperinsulinism / Q000150:complications; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology* / Q000517:prevention & control; D020738:Leptin / Q000378:metabolism; D009765:Obesity / Q000150:complications* / Q000503:physiopathology*; D012307:Risk Factors; D020181:Sleep Apnea, Obstructive / Q000209:etiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D015431:Weight Loss
D058667:Adrenergic beta-3 Receptor Agonists; D020738:Leptin